The present invention relates to a composition for the treatment of rashes, dermatoses or skin eruptions, which are known to be treated topically to improve or favorably alter the disease condition. Such rashes, dermatoses or skin eruptions include acute, inflammatory reactions of the skin caused by an allergic or irritant reaction (such as that caused by poison ivy, poison oak or poison sumac, or other forms of allergic or irritant contact dermatitis), other forms of eczema, lichen simplex chronicus, rashes, dermatoses or skin eruptions of a chronic nature (e.g. seborrheic dermatitis, psoriasis, atopic dermatitis) or caused by infection, irritation or aggravation of another condition such as occurs with acne, and other rashes, dermatoses or skin eruptions.
Contact dermatitis may be produced by primary irritants or allergic sensitizes. Irritant contact dermatitis is a nonallergic reaction of the skin caused by exposure to irritating substances. Any person would react to an irritant if the concentration and duration of contact were sufficient. Most primary irritants are chemical substances, although physical and biologic (infectious) agents may produce the same reaction. Irritants account for 80% of occupational contact dermatitis and also cause the most frequent type of nonindustrial contact reaction. Allergic contact dermatitis is a manifestation of delayed hypersensitivity and results from the exposure of sensitized individuals to contact allergens. Poison ivy and poison oak induce sensitization in more than 70% of the population, thereby causing allergic contact dermatitis (Arndt, Kenneth A., Manual of Dermatologic Therapeutics, 5th edition, 1995, Little, Brown and Co., page 49).
Irritants will cause an inelastic and stiff-feeling skin, discomfort due to dryness, pruritus secondary to inflammation, and pain due to fissures, blisters, and ulcers. Mild irritants produce erythema, microvesiculation, and oozing that may be indistinguishable from allergic contact dermatitis. Chronic exposure to mild irritants or allergens results in dry, thickened, and fissured skin. Strong irritants cause blistering, erosion, and ulcers of the skin. Allergic contact dermatitis, in its mild form, is similar in appearance to the irritant eruption. A more typical allergic contact reaction will consist of grouped or linear tense vesicles and blisters. If involvement is severe there may be marked edema, particularly of the face and in the periorbital and genital areas.
A variety of methods exist for treating contact dermatitis, including topical corticosteroids, aluminum acetate (Burow's solution), soothing shake lotions (e.g. calamine lotion), oral antihistamines, and systemic corticosteroids. Individually these therapies do not bring rapid relief of all the symptoms of pruritus (itch), the inflammation of the dermatitis, as well as vesiculation and oozing. Usually combination therapy is preferred.
Systemic corticosteroids will cure most cases of contact dermatitis, no matter how severe. But initial dosage should be 60 mg of prednisone daily (or an equivalent strength of another form of corticosteroid), and the course should be no shorter then 2-3 weeks. There are many contraindications to corticosteroid treatment. Absolute contraindications include ocular herpes simplex and untreated tuberculosis. Relative contraindications include acute or chronic infections, pregnancy, diabetes mellitus, hypertension, peptic ulcer, osteoporosis, psychotic tendencies, renal insufficiency, congestive heart failure, and recent intestinal anastomoses (Arndt, Kenneth A., Manual of Dermatologic Therapeutics, 5th edition, 1995, Little, Brown and Co., page 309). There are many common corticosteroid complications, including psychiatric disorders, pseudotumor cerebri, osteoporosis with spontaneous fractures, aseptic necrosis of bone, myopathy, glaucoma, cataracts, fatty infiltration of the liver, intestinal perforation, pancreatitis, peptic ulceration, hypertension, sodium and fluid retention, hypokalemic alkalosis, atherosclerosis, immunosuppression, increased incidence of infections, suppression of the hypothalamic-pituitary-adrenal axis, growth failure, and inhibition of wound healing. So, while the clinical results from systemic corticosteroid use are encouraging, a more rapid and complete clinical response with less risk of side effects is desired.
Topical corticosteroids will eradicate a case of contact dermatitis, but will not rapidly stop new vesicles from forming or dry up oozing, weeping patches and vesicles rapidly. While these results are encouraging, a more rapid and complete clinical response is desired.
Soothing lotions (e.g. calamine lotion) and other drying agents such and aluminum acetate (Burow's solution) will dry oozing, weeping patches, vesicles and erosions. But when used alone they typically do not provide relief from the inflammation caused by the dermatitis. Again, while these results are encouraging, a more rapid and complete clinical response is desired.
None of the above agents provide rapid drying of a moist, oozing rash while helping to absorb further moisture and keep the skin dry, and at the same time treat the contact dermatitis.
There are several other papulosquamous skin diseases that can present and behave in a similar fashion to contact dermatitis. These include all other forms of eczema, lichen simplex chronicus, rashes, dermatoses or skin eruptions of a chronic nature (e.g. seborrheic dermatitis, psoriasis, atopic dermatitis), and others. All of these conditions can present with a rash that can become moist, weeping, and quite irritated. The rashes can also become secondarily infected. Current therapeutic options do not always clear these conditions as rapidly as desired.